cattle under 30 months of age present no risk of harboring BSE prions andthus, cannot cause vCJD in humans.

22. Prion diseases are invariably fatal and no vaccine, antidote or cureexists to treat them. Similar to the human prion disease, it is likely thatthe spontaneous (or sporadic) for of BSE accounts for many cases in cattleand thus prions will not disappear from livestock simply by eliminatingprion-infected feeds. That being the case, it is imperative for the USDA toimplement measures that address this public health thread and mitigate therisk of transmission as much as possible which should include the testing ofall cattle slaughtered in the United States.

I declare under penalty of perjury under the laws of the United States ofAmerica that the foregoing is true and correct. Executed on June 28, 2005

NO wonder my PDF reader would not read the rest of Stans testimony, justmore BSe about spontaneous BSE/TSE with absolutely no proof what so everythat many cases of any TSE arises spontaneously. PDF reader did not believeit either. but would be a handy tool to sell more rapid tests. i cannotbelieve i said that, but there is absolutely no science to support stans'claim that ;

>Similar to the human prion disease, it is likely that the spontaneous (orsporadic) for of BSE accounts for many cases in cattle...<

IF the incubation times, the neuropathological lesion profiles, and theGdn1/2 values indicate that MoSP1 test tube prions differ from RML and manyother prion strains derived from sheep with scrapie and cattle with bovinespongiform encephalopathy, then what proof does Stan have that in deed ;

>Similar to the human prion disease, it is likely that the spontaneous (orsporadic) for of BSE accounts for many cases in cattle...<

http://www.vegsource.com/talk/madcow/messages/94634.html

Conclusions and perspectivesThe nature of the infectious agent associated with TSE has been one of themost heated debates in the biological sciences. The evidence in favor of theheretical protein-only hypothesis is extensive and is transforming the prionconcept into a new dogma with vast implications for diverse areas ofbiology. Prions, defined as infectious proteins with the ability to transmitbiological information through the propagation of alternative proteinfolding, represent an entirely new mechanism for expanding phenotypicdiversity without changes in the genome2, 51. Skeptics argue, however, thatthe prion hypothesis is still not definitively proven32, 38. It is widelyagreed that the final proof of the protein-only hypothesis will require theengineering in vitro of a synthetic infectious protein capable ofpropagating a prion in vivo. These experiments have now been completedsuccessfully using the yeast prion Sup35 protein54, 55, coming tantalizinglyclose to be the long-awaited definitive proof of the prion hypothesis. Butdo these studies demonstrate that prions are the infectious agentsassociated with TSEs? No—they demonstrate that the biological principleunderlying prions is correct and that the nature of the strain phenomenonindeed resides in the propagation of alternative protein folding. However,the challenge of transmitting disease for an infectious agent composed onlyof a protein is greater in a multicellular organism than in yeast. Theprotein must resist biological clearance mechanisms, get to the right placein the brain, be propagated from cell to cell and induce specific cerebraldamage that is different depending on the exact folding of the infectiousagent. Until successful generation of infectivity by in vitro production oramplification of PrPres can be demonstrated, it remains possible thatmisfolded PrP is not the only component of the prion infectious agent.

http://www.nature.com/nm/journal/v10/n7s/full/nm1069.html

4:15 Disease Phenotype and Transmission Properties of Bovine AmyloidoticSpongiform EncephalopathyDr. Gianluigi Zanusso, University of Verona, ItalyBy active surveillance system on BSE, two cows of 11 and 15 years with apreviously unrecognized form of prion disease (bovine amyloidotic spongiformencephalopathy or BASE) were recognized. Differently from typical BSE thisnovel form is characterized by the presence of PrP positive plaques andmolecular PrPSc characteristics similar to those encountered in a distinctsubtype sCJD. An update on strain characterization upon transmissionexperiments will be presented.

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsiblefor French iatrogenic growth hormone-linked CJD taken as a control isvery different from vCJD but is similar to that found in one case ofsporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strainsderived from bovine spongiform encephalopathytransmissions to inbred mice